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Three major theories exist explaining the pathophysiology of Charcot arthropathy:

Neurotraumatic theory (German): A joint without proper sensory innervation is subject to repeated injury. The patient is unaware of minor trauma to the joint and continues to damage it over time.

Neurovascular theory (French): Loss of sympathetic vascular tone leads to increased blood flow to the joint, causing an imbalance in bone metabolism. Over time the joint becomes osteopenic

Modern theory: A combination of the previous two theories.

Both the neurotraumatic and neurovascular mechanisms are likely to be involved and complement each other. The joint, mechanically weaker due to bone loss is subject to repeated minor injuries, and the patient is unaware of the destruction until the joint is badly damaged.

The clinical presentation varies depending on the stage of the disease from mild swelling to severe swelling and moderate deformity. Inflammation, erythema, pain and increased skin temperature (3-7 degrees celsius) around the joint may be noticeable on examination. X-rays may reveal bone resorption and degenerative changes in the joint. These findings in the presence of intact skin and loss of protective sensation are pathognomonic of acute Charcot arthropathy.

Roughly 75% of patients experience pain, but it is less than what would be expected based on the severity of the clinical and radiographic findings.

Treatment is usually non-operative, consisting of reduction of stress on the joint by casting, avoiding weight bearing where possible, and elevation to reduce blood flow (decreasing inflammation and bone loss). Only about 25% of cases require surgery.

Outcomes vary depending on the location of the disease, the degree of damage to the joint, and whether surgical repair was necessary. Average healing times vary from 55–97 days depending on location. Up to 1–2 years may be required for complete healing.